Stampfer D S, McDougal W S
Department of Urology, Massachusetts General Hospital, Boston 02114, USA.
J Urol. 1997 Jan;157(1):362-5.
Previous work from our laboratory suggests that one mechanism of ammonium transport across the intestinal membrane may be substitution of ammonium for sodium in the sodium/hydrogen antiport. This study further supports this mechanism by demonstrating an inhibitory role for ammonium in the sodium/hydrogen exchange.
Whole brush border intestinal enterocytes were studied, incorporating a fluorescent marker for sodium transport. The kinetics of the effect of ammonium on sodium transport were determined.
Ammonium is an inhibitor of sodium in the sodium/hydrogen exchanger. Quantitatively, the inhibition appears to be competitive.
The inhibitory effect of ammonium on sodium/hydrogen exchange supports a mechanism of ionized ammonium transport where it substitutes for sodium in the sodium/ hydrogen exchanger. This is a mechanism by which hyperchloremic metabolic acidosis occurs following urinary intestinal diversion.
我们实验室之前的研究表明,铵跨肠膜转运的一种机制可能是在钠/氢逆向转运体中铵替代钠。本研究通过证明铵在钠/氢交换中的抑制作用进一步支持了这一机制。
研究了完整的刷状缘肠上皮细胞,其中加入了用于钠转运的荧光标记物。测定了铵对钠转运影响的动力学。
铵是钠/氢交换体中钠的抑制剂。从数量上看,这种抑制似乎是竞争性的。
铵对钠/氢交换的抑制作用支持了离子化铵转运的一种机制,即它在钠/氢交换体中替代钠。这是尿流改道后发生高氯性代谢性酸中毒的一种机制。